Filkins J P, Figlewicz D P
Circ Shock. 1979;6(1):1-6.
The relation of endotoxicosis to insulin responsiveness was evaluated in male Holtzman rats. Salmonella enteritidis lipopolysaccharide at 0.5 or 1.0 mg per 300 g rat increased lethality in convulsive seizure deaths to 0.25, 0.50, or 1.0 U insulin sc. The hypoglycemic nadir induced by 0.05, 0.10, or 0.25 U of insulin sc was greater in rats rendered endotoxic with 1 mg of lipopolysaccharide IV. Oxidation of U-14C-D-glucose to 14 CO2 by endotoxic tissues in vitro was augmented in liver slices, epididymal fat pads, hemidiaphragms, and spleen slices; no pronounced glucose oxidation increases occurred in lung, heart, stomach, cerebrum, kidney, or whole blood. Epididymal fat pads from endotoxic rats (100 g) manifested increased basal glucose oxidation as well as an enhanced maximal response to incremental insulin doses of 0.01 to 25 mU/ml. It is suggested that altered tissue responsiveness in concert with hyperinsulinemia underlie the profound alterations in glucose homeostasis during endotoxicosis.
在雄性霍尔兹曼大鼠中评估了内毒素血症与胰岛素反应性的关系。每300克大鼠给予0.5或1.0毫克肠炎沙门氏菌脂多糖，可使惊厥性癫痫死亡的致死率增加至皮下注射0.25、0.50或1.0单位胰岛素的情况。静脉注射1毫克脂多糖使大鼠产生内毒素血症后，皮下注射0.05、0.10或0.25单位胰岛素所诱导的低血糖最低点更低。体外实验中，内毒素血症大鼠的组织（肝脏切片、附睾脂肪垫、半膈肌和脾脏切片）将U-14C-D-葡萄糖氧化为14CO2的能力增强；而肺、心脏、胃、大脑、肾脏或全血中未出现明显的葡萄糖氧化增加。内毒素血症大鼠（100克）的附睾脂肪垫基础葡萄糖氧化增加，对0.01至25毫单位/毫升递增胰岛素剂量的最大反应也增强。提示在内毒素血症期间，组织反应性改变与高胰岛素血症共同构成了葡萄糖稳态深刻变化的基础。
